INCIDENCE AND OUTCOMES OF PULMONARY COMPLICATION AFTER CARDIAC SURGERY

LITHUANIAN UNIVERSITY OF HEALTH SCIENCES

MEDICAL ACADEMY FACULTY OF NURSING

DEPARTMENT OF NURSING AND CARE

LINTA MARIAM YOHANNAN

INCIDENCE AND OUTCOMES OF PULMONARY

COMPLICATION AFTER CARDIAC SURGERY

The graduate thesis of the Master‘s degree study programme “Advanced Nursing Practice” (State Code 6211GX008)

Tutor of the graduate thesis PhD MD, Judita Andrejaitienė

TABLE OF CONTENT

ABSTRACT………..3

ABBREVIATIONS.……….…...4

INTRODUCTION……….………...…...5

1. REWIEW OF LITERATURE..………... ...7

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Pulmonary Pathophysiology……….………...7

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Pulmonary Complications……….………..…………...………...7

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Risk Factors For Pulmonary Complications…...16

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Management………..………...17

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Physiotherapy………..………...24

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Prone Position………...26

2. ORGANISATION AND METHODOLOGY OF A RESEARCH...27

3. RESULTS…….………...…....27

4. DISCUSSIONS…….………..………...…...30

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CONCLUSIONS………..………...…...35

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PRACTICAL RECOMMENDATIONS……..………...36

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PUBLICATIONS………..………...…….37

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LIST OF LITERATURE SOURCES…..…………..……...……...38

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ANNEXES………..………...………...42

DECLARATION OF THE AUTHOUR’S CONTRIBUTION AND

ABSTRACT

Linta Mariam Yohannan. Incidence and outcomes of pulmonary complication after cardiac surgery.

The graduate Master‘s thesis. The tutor-PhD MD Judita Andrejaitienė. Lithuanian University of Health Sciences, Medical Academy, the Faculty of Nursing, Department of nursing and care. Kaunas, 2019;43p.

AIM: To analyse the incidence and outcome of pulmonary complication after cardiac surgery, OBJECTIVES: *To determine the incidence of pulmonary complications after open cardiac surgery.

*To identify predisposing risk factors of these complications. *To research outcomes of pulmonary complication. *To analyse preventive and treatment strategy. METHODOLOGY OF

ORGANISATION: The literature search was performed in the databases PubMed, Science Direct,

PLOS Google Scholar. Reviewed more than 40 literature reviews, published between 2009-2019. The analysis of the case report and the PICO questionnaire method is thoroughly performed in the literature review. CONCLUSION: *PPC is a quite common complication after cardiac surgery, whose incidence still remains unacceptably high nowadays. Literary review recommends the use numerous therapeutic measures that minimize PPD after cardiac surgery. *It is very important to the patients with severe ARDS who are receiving MV support to apply OLV strategy that combines LTVV with a recruitment maneuver and subsequent titration of applied PEEP to maximize alveolar recruitment, and next steps to improve hypoxemia - prone positioning (PP). *Early application PP has shown to be effective in reducing atelectasis and PPD, minimizing re-intubation rates, length of stay in ICU, and hospital and ICU readmissions.

ABBREVIATIONS

ARDS Acute respiratory distress syndrome CPB Cardiopulmonary bypass

CAD Coronary artery disease ICU Intensive care unit

OLA Open lung approach MV Mechanical ventilation

PPCs Postoperative pulmonary complications VAP Ventilator-associated pneumonia

MHS Major heart surgery NIV Non-invasive ventilation PP Prone positioning.

Paco2 Arterial oxygenation Fio2 Fractions of inspired oxygen

PEEP Positive end-expiratory pressure IBW Ideal body weight

INTRODUCTION

Postoperative pulmonary dysfunction (PPD) is a frequent and significant complication after cardiac surgery. PPD clinical manifestations include atelectasis (16.6–88%) and postoperative hypoxemia without clinical symptoms (3–10%) and acute respiratory distress syndrome (ARDS), which have a low incidence (0.5–1.7%) but high mortality (50–90%) [5]. PPD pathogenesis is not clear but it seems to be related to the development of a systemic inflammatory response with a subsequent pulmonary inflammation. Many factors have been described to contribute to this inflammatory response, including surgical procedure with median sternotomy incision, effects of general anesthesia, hypothermia for myocardial protection and cardiopulmonary bypass (CPB), dissection of the internal mammary artery and mechanical ventilation (MV). Protective ventilation strategies can reduce the incidence of atelectasis (which still remains one of the principal causes of PDD) and pulmonary infections in surgical patients. In this way, the open lung approach (OLA) [6], a protective ventilation strategy, has demonstrated attenuating the inflammatory response and improving gas exchange parameters and postoperative pulmonary functions [5].

Pulmonary dysfunction remains a potential complication after cardiac surgery. The cost of health care and mortality may increase over the duration of the hospital and the intensive care unit. Pulmonary complications significantly contribute to early morbidity of the heart. According to Le H, Janelle GM et al. [3], Studies have also shown that 5-8% of deaths after cardiac surgery can be attributed to pulmonary causes. In addition to intraoperative factors such as physical lung manipulation, inflammation-related cardiopulmonary bypass (CPB), fluid management, and postoperative factors such as weaning strategy, cardiac function, mobilization, and pain control, the risk of pulmonary complications is associated with chronic preoperative lung disease, smoking, higher age, and frailty. Miskovic A et al [4]. The task force considered composite measures and defined pneumonia, acute respiratory distress syndrome (ARDS) and pulmonary embolus as individual adverse outcomes of respiratory infection, respiratory failure, pleural effusion, atelectasis, pneumothorax, bronchospasm, and aspiration pneumonitis. Postoperative studies of pulmonary complications also use different combinations of these outcomes. A systematic review for the American College of Physicists showed that almost 60% of 16 studies used a combination of pneumonia and respiratory failure to define pulmonary system postoperative complications. Pulmonary complications are costly and require hospitalization for a long time. The National Surgical Quality Improvement Program (NSQIP) compared hospitalization costs and length of stay among patients with different postoperative complications. Pulmonary complications between infectious, cardiovascular, venous

thromboembolic and pulmonary complications were by far the most expensive and required the longest average hospital stay together with venous thromboembolic complications.

Acute respiratory distress syndrome (ARDS) is a leading cause of postoperative respiratory failure, with a mortality rate approaching 40% in the general population and 80% in the cardiac surgery subset of patients. In these patients, the increased risk of ARDS has traditionally been associated with the use of cardiopulmonary bypass (CPB), the need for transfusions of blood product, large volume shifts, mechanical ventilation and direct surgical insult. Indeed, the effect of ARDS on the cardiac population is significant, influencing not only survival but also the length of stay in hospital and long-term physical and psychological morbidity.

Postoperative pulmonary dysfunction (PPD) is a frequent and significant complication after cardiac surgery. PPD clinical manifestations include atelectasis (16.6–88%) and postoperative hypoxemia without clinical symptoms (3–10%) and acute respiratory distress syndrome (ARDS), which have a low incidence (0.5–1.7%) but high mortality (50–90%) [5]. PPD pathogenesis is not clear but it seems to be related to the development of a systemic inflammatory response with a subsequent pulmonary inflammation. Many factors have been described to contribute to this inflammatory response, including surgical procedure with median sternotomy incision, effects of general anesthesia, hypothermia for myocardial protection and cardiopulmonary bypass (CPB), dissection of the internal mammary artery and mechanical ventilation (MV). Protective ventilation strategies can reduce the incidence of atelectasis (which still remains one of the principal causes of PDD) and pulmonary infections in surgical patients. In this way, the open lung approach (OLA) [6], a protective ventilation strategy, has demonstrated attenuating the inflammatory response and improving gas exchange parameters and postoperative pulmonary functions [6].

AIM:

 To analyse the incidence and outcome of pulmonary complication after cardiac surgery.

OBJECTIVES:

 To determine the incidence of pulmonary complications after open cardiac surgery.

 To identify predisposing risk factors of these complications.

 To research outcomes of pulmonary complication.

1. REVIEW OF LITERATURE

Pulmonary pathophysiology

In the very nature of traditional heart surgery median sternotomy, CPB, depressed heart function and thoracic content manipulation pulmonary and cardiac mechanics are altered. The pulmonary issues following this procedure include secondary cardiac dysfunction (pulmonary edema and congestive cardiac failure), intrinsic lung disorders (e.g. atelectasis and pneumonia), and CBP (acute respiratory distress syndrome). Pulmonary dysfunction from fever and productive coughing to respiratory failure requiring prolonged mechanical ventilation is the result of clinical manifestations of post cardiac surgery. Cardiac dysfunction is the leading cause of poor lung outcomes after cardiac surgery. This finding is not unexpected since low cardiac output states contribute to lung dysfunction directly and indirectly. The low heart output increases pulmonary capillary pressure and lungs water, leading to difficulties ranging from mild heart failure to open cardiovascular pulmonary edema. In addition, low cardiac output leads to fatigue, leading to weak coughing, reduced mobility and lack of deep breathing. These conditions can exacerbate atelectasis and strengthen pneumonia propensity.

Pulmonary Complications

Atelectasis

The most frequent pulmonary consequence of cardiac surgery is atelectasis, seen on postoperative chest radiographs in approximately 50% to 90% of patients [7]. Operation is a major risk factor for atelectasis. Coughing is not possible for these patients, and suctioning by nurses is not as effective as coughing for atelectasis prevention. It helps to prevent atelectasis by taking a deep breath and cough. Atelectasis can be a minor complication, but when the patient has other serious problems after cardiac surgery, it can become a very serious complication. An individual who is kept on a ventilator after cardiac surgery is probably already very ill and atelectasis can be an undesirable complication because it can lead to more serious lung problems than those that already exist. The condition can mean that too little oxygen reaches the body for patients who have already compromised lung function, such as an individual who has lung cancer, or who has only one lung. Atelectasis is not always serious, a very small area of atelectasis may not be a problem for most people, but if large areas of one or both lungs are affected, the condition may be life-threatening and requires immediate and aggressive treatment [19]. There are many postoperative causes of atelectasis following cardiac surgery, including poor postoperative coughing, lack of deep inspiration, pleural effusions, stomach distention, and increased

interstitial lung water. Both pain and mechanical / neural changes are responsible for the increased respiratory rate and shallow breaths that often characterize the postoperative spontaneous respiratory pattern. This pattern contributes to the formation of atelectasis.

Respectively intraoperative and postoperative etiologies may cause atelectasis. Intraoperative effects include general anesthesia induction, manual lobe compression during maneuvers to reveal the posterior surface of the heart, manual compression of the right lung during inferior venacava cannulation, manual lung compression throughout internal mammary artery dissection, and apnea during cardiopulmonary bypass.

Evaluation of the air bronchograms in the chest can help determine if the airway obstruction is proximal or distal. Patients with mucous airway plugging may benefit from chest physiotherapy, nebulized dornase alfa (DNase), and possibly fiber optic bronchoscopies. A positive final expiratory pressure may be a useful addition to the treatment in passive and adhesive atelectasis.

After thoracic or upper abdominal procedures, atelectasis may occur postoperatively. Although atelectasis is seen as the most frequent cause of early after operative fever, there is contradictory evidence. In a study, no clinical evidence supporting the concept of early post-operative fever associated with atelectasis. The velocity of bronchial occlusion, the size of the lung area affected as well as the presence or absence of complex infection determine most symptoms and signs. Rapid bronchial occlusion with a wide area of lung collapse causes pain on the affected part, dyspnea and cyanosis suddenly occurring. There may also be hypotension, tachycardia, fever, and shock. Atelectasis may develop slowly asymptomatically or may only cause minor symptoms. Middle lobe syndrome is often asymptomatic, although irritation can cause severe, hacking, nonproductive cough in the right middle and right lobe bronchi.

Haemothorax and pleural effusions

Pleural effusions are seen on immediate postoperative chest radiographs in the majority of patients. Additionally, 10% to 40% of patients develop pleural effusions 2 to 3 weeks after surgery secondary to postpericardiotomy syndrome. While some effusions require drainage and further intervention (eg, hemothorax), most effusions require no specific treatment and resolve over time Christopher Noel [12].

The causes of these effusions include postoperative bleeding, atelectasis, pneumonia, cardiogenic and non - cardiogenic pulmonary edema, pleurotomy performed for the harvesting of internal mammary

arteries, damage caused by topical cardiac hypothermia, disruption of pleural lymphatic drainage by the harvesting of internal mammary arteries, and fluid leakage from mediastinum.

The majority of the effusions were left-sided, small, asymptomatic and spontaneously resolved.With CABG performed with internal mammary arteries, the prevalence of pleural effusions is higher than only saphenous vein grafts. Some CABG patient develops large pleural effusion (more than 25% of haemothorax), they tend to be one sided and left-sided. Some are bloody, have a high number of eosinophils, reach their maximum volume one month after surgery and are believed to be caused by bleeding into pleural space.

Pneumothorax

In the five year study period, 8900 patients underwent cardiac surgery. There were 6236 males and 2542 females with 66.5 years of average age. Postoperative pneumothorax suffered one hundred and twenty - two patients for a total incidence of 1.4% [6].

Due to direct lung injury during surgery or central venous cannulation, spontaneous rupture of pulmonary blebs, and barotrauma during mechanical ventilation, pneumothoraces may occur after cardiac surgery. In the chest cavity, mediastinal and often pleural tubes are routinely placed to evacuate air and blood immediately before closing the chest. Pneumothoraces can occur immediately after surgery, however, when air accumulates in unopened pleura surrounding damaged lung tissue.

Pneumonia

Hospital-acquired (or nosocomial) pneumonia (HAP) is pneumonia that occurs 48 hours or more after admission and did not appear to be incubating at the time of admission.

Ventilator-associated pneumonia (VAP) is a type of HAP that develops ≥48 hours after endotracheal intubation [8].

VAP and other complications are at high risk for mechanical ventilation patients. It is difficult to determine the true incidence of VAP because definitions of surveillance are subjective and non-specific. Historically, VAP has been developed by 10%-20% of ventilated patients. Nosocomial pneumonia is common among patient with ADRS.

The prevalence of pneumonia varies based on differences in study populations and diagnostic criteria, but remains an important source of morbidity and mortality. Postoperative pneumonia occurred in

one series in 3.1% of patients, with higher rates observed in older patients, lower left ventricular ejection fraction, COPD, longer bypass times, and more red blood cell transfusions in the operating room, its incidence ranges from 2% to 22% following cardiac surgery. This wide range results from various populations of study and pneumonia definitions. 3.8% of the studied population developed ventilator-associated pneumonia (VAP) in a multicenter European study. Patients who have been mechanically ventilated for at least two days are diagnosed with VAP. Clinical, radiographic and bacteriological criteria are the diagnostic criteria recommended by the European Center for Disease Control (ECDC) [1].

Ventilator-associated pneumonia (VAP) is one of the most common nosocomial infections in critically ill patients, defined as pulmonary infection that develops 48 hours or more after mechanical ventilation. It is reported that VAP is responsible for a significant increase in mortality and morbidity and is associated with the highest costs resulting from prolonged hospitalization. Patients who have undergone cardiac surgery and stay in the intensive care unit (ICU) generally require long-term mechanical ventilation [6].

Eleven studies on VAP after cardiac surgery were included. The prevalence reached 6.37% of all patients and 35.2% of patients who were on mechanical ventilation for more than 48 hours. Among the isolated pathogens, Pseudomonas aeruginosa had the highest detection rate, with an average of 23.19%, followed by Staphylococcus aureus (20.15%), Haemophilus influenza (19.53%), Acinetobacter baumannii (10.68%), Escherichia coli (10.18%), Klebsiella pneumoniae (9.52%), and Candida albicans (7.20%). We found that New York Heart Association cardiac function class IV, pulmonary hypertension, chronic obstructive pulmonary disease, peripheral vascular disease, renal disease, emergency surgery, intra-aortic balloon counter pulsation, cardiopulmonary bypass time, aortic cross clamp time, mechanical ventilation time, reintervention, and reintubation were closely related to the occurrence of VAP; Once patients had VAP, mortality and length of stay in the intensive care unit were significantly increased.VAP in patients after cardiac surgery is common and has a poor prognosis [8].

The development of VAP in MHS patients has been related to different risk factors, including time of mechanical ventilation, need for reintubation, transfusion needs, empirical use of broad spectrum antibiotics, type of surgery, age over 60 years, supine position for the first 24 hours, history of chronic obstructive pulmonary disease [7].

Unfortunately, most variables that significantly predict VAP are not likely to intervene. We believe the use of anticipatory or preventive antimicrobial therapy should be considered as one of the only

possible interventions to prevent VAP in the high-risk population. Inadequate empirical therapy is known to be associated with increased VAP mortality, although correction occurs within the following hours. Singh and his colleagues showed that three days of ciprofloxacin administration in patients with suspicion of VAP have a very favorable effect on the cost and duration of antimicrobial use and have reduced reinfection rates and resistance. In addition, the use of oral decontamination and three days of cefotaxime or ceftriaxone have shown that antimicrobial pre-prevention therapy can potentially be beneficial in patients with high VAP risk [7]. Pneumonia, pulmonary oedema, atelectasis and acute respiratory distress syndrome are the most common causes of VACs. Consequently, interventions aimed specifically at these complications and interventions designed to shorten the mechanical ventilation duration in general can be effective strategies for lowering VAE rates. These could include reducing the use of sedatives, pairing daily spontaneous awakening and breathing tests, early mobility, endotracheal tubes with subglottic secretion drainage ports, low tidal volume ventilation, intermittent recruitment maneuvers, conservative fluid management, and restrictive transfusion thresholds. The benefits of oral care with chlorhexidine appear to be most pronounced in preventing postoperative respiratory tract.

Pathophysiology

The invading organism begins to multiply, releasing toxins that cause lung parenchyma inflammation and edema. This leads to cellular debris accumulation in the lungs. This results in consolidation or solidification, a term used for the macroscopic or radiological appearance of pneumonia-affected lungs.

The main classification of bacterial pneumonia is lobar and lobular penumonia. In the alveoli, lobar pneumonia begins and spreads through Kohn's pores. In the terminal and respiratory bronchioles, on the other hand, lobular pneumonia (bronchopneumonia) begins and spreads through the bronchial walls into the alveoli.

In case of lobar pneumonia, one or more lung lobes could be homogeneously consolidated. Bronchopneumonia, on the other hand, is characterized by patchy consolidation of alveolar and bronchial inflammation, which often involves both lobes.

Management

 Antibiotic

 Physiotherapy when tenacious sputum or mucus plugging.

 Oxygen as appropriate to achieve the following target oxygen saturation: 94-98% for most patients 88-92% for those with COPD or at risk of hypercapnic respiratory failure (e.g. morbid obesity, neuromuscular or chest wall disease).

 IV fluids if appropriate (fever / excess fluid loss).

 Repeat CXR and CRP and consider early respiratory referral if not improving within 3 days.

Prevention of ventilator associated pneumonia

 Avoid intubation if possible. (Use noninvasive positive pressure ventilation (NIPPV)).

 Minimize sedation. (Manage ventilated patients without sedatives whenever possible).

 Maintain and improve physical conditioning. (Provide early mobilization and exercise. Early exercise and mobilization speed extubation, the length of stay decreases and the rate of return to independent function increases).

 Minimize pooling of secretions above the endotracheal tube cuff. (Provide subglottic secretion drainage ports for endotracheal tubes that may require more than 48 or 72 hours of intubation).

 Maintain ventilator circuits. (Change the ventilator circuit only if visibly soiled or malfunctioning).

Adult respiratory distress syndrome

The incidence of adult respiratory distress syndrome (ARDS) after cardiac surgery is between 0.4% and 4%. The syndrome may be caused by physical compression of the lungs, discontinuation of ventilation, blood transfusion and, more importantly, CPB.

When used several days after the onset of the disease, the prone position can effectively increase oxygenation and its application in the early stages has been found to offer better results. All conditions favoring pronation efficacy are present during these early stages, such as alveolar edema, reversible collapse, and the absence of structural pulmonary alterations. The reduction in the risk of ventilator-associated lung injury in these stages is likely to exceed that obtained when pronation is used in later stages of ARDS, where the damage has already been caused. This was clearly shown in our study, where patients in the prone position within the first 48h of disease evolution showed a clear protective effect referring to mortality risk. In clinical practice, the severity of ARDS was rated according to the

ratio of PaO2/FiO2, although in disorders as complex as this syndrome, the ratio of PaO2/FiO2 depends on the level of PEEP and FiO2 administered, as well as the treatments and/or interventions prescribed, the comorbidities and the disease's innate compensatory mechanisms. Despite the presence of these variables, the results obtained allow us to clearly show that the prone position is indicated in patients with severely impaired oxygenation, as has already been shown in other studies. In addition, prolonging the prone position to more than 12 consecutive hours per day (average 18 hours) in patients with severe ARDS is a highly recommended strategy. It is important to note that pronation was not found to offer clinical advantages in patients with mild ARDS and is therefore not recommended. The clinical recommendation for moderate ARDS is also not clear, although the post-hoc analysis results of a meta-analysis 9 revealed a certain tendency to benefit patients with PaO2/FiO2<140.

Airway pressure release ventilation (APRV) mode of mechanical ventilation is an elevated CPAP level with timed pressure releases. This mode allows for spontaneous breathing. These breaths can be unsupported, pressure supported, or supported by automatic tube compensation. They key is a dynamic expiratory valve in the circuit which allows spontaneous breathing at high lung volumes. While any patient can be adequately supported using APRV, it is generally used for patients the require recruitment of alveoli to maintain oxygenation, such as in ARDS (along with other treatment such as inhaled prostacyclin, neuromuscular blocked, PEEP, and prone position.)

Pathophysiology

Increased pulmonary microvasculature permeability causes protein fluid leakage across the alveolar-capillary membrane. This may be a manifestation of a more widespread endothelium disruption, leading to hypoxia and multiple organ failure. The production of surfactants also decreases. Some patients are progressing to fibrosis while others are recovering.

The hallmark of ARDS is increased capillary permeability. Damage to capillary endothelium and alveolar epithelium in correlation with impaired fluid removal from alveolar space results in the accumulation of protein-rich fluid within alveoli, resulting in diffuse alveolar damage resulting in the release of pro-inflammatory cytokines such as Tumor Necrosis Factor (TNF),IL-1andIL-6. Cytokines recruit neutrophils into the lungs, activate them, and release toxic mediators like reactive oxygen species and proteases. Large free production of radicals overwhelms endogenous antioxidants and causes oxidative cell damage.

Inflammation due to activation of neutrophils is key to ARDS pathogenesis. Fundamental transcription abnormalities involving NF-kappa B, which many pro-inflammatory mediators require for gene transcription, are present in ARDS patients ' lungs. Other factors such as endothelin-1, angiotensin-2 and phospholipaseA-2 also increase vascular permeability and destroy micro-vascular architecture, increasing inflammation and damage to the lungs. In conclusion, since the development of ARDS involves several different pathways, no single biomarker can predict results in ARDS patients.

In the 1980s, computed tomography studies helped us to understand the pathophysiological changes in ARDS patient’s lungs. Furthermore, since lung compliance correlates with the degree of normal ventilated tissue, lung compliance in ARDS decreases due to reduced lung size rather than lung stiffness, and this hypothesis introduced the concept of "baby lung" in ARDS.

Initial Ventilator Management in ARDS

The following approach is generally recommended for ARDS ventilator management:

 Assist-control mode is initially used with an ideal body weight of 6mL / kg, respiratory rate 25/min, flow rate 60 L / min, Fio2 1.0 and PEEP 15cm H2O. Once the saturation of oxygen is >90%, Fio2 is reduced.

 PEEP is then reduced in increments of 2.5cm H2O as tolerated to find the least PEEP associated with 90% arterial oxygen saturation on a Fio2 of ≤ 0.6.

 To achieve a pH of >7.15, the respiratory rate is increased up to 35/min, or until the expiratory flow tracing shows end-expiratory flow.

Ideal body weight (IBW) is used to determine the appropriate tidal volume for mechanically ventilated patients with lung disease.

IBW (kg) Males: 50 + 2.3(heights in inches - 60) or 50 + 0.91 (height in cm - 152.4) IBW (kg) Females: 42.5 + 2.3(height in inches - 60) or 45.5 + 0.91(height in cm - 152.4)

Corticosteroids and exogenous surfactant treatments were evaluated because the characteristics of ARDS are inflammation and changes in surfactant function. Before the onset of ARDS or during its early course, methylprednisolone does not decrease mortality. Results from a recent small randomized trial, however, showed significant mortality improvement when corticosteroid therapy was initiated seven days after diagnosis.

Most ARDS patients need sedation to facilitate synchrony between patient and ventilator and to reduce oxygen demand. Neuromuscular blocking agents are sometimes required to provide effective ventilation, but their use should be limited given the short-and long-term effects of these agents and the depth of the paralysis should be carefully monitored.

Complication of ADRS

 Tracheal stenosis, vocal cord dysfunction

 Ventilator-associated pneumonia

 Gastrointestinal

 Stress-related gastrointestinal hemorrhage

 Pneumothorax, Pneumomediastinum, Pneumoperitoneum, Air embolism.

 Cardiac/hemodynamic.

 Excessive sedation

 Mechanical damage from central line placement. And others.

Prevention of ADRS

 Use of stress ulcer prophylaxis

 Identify appropriate time for tracheostomy.

 Head elevation, suctioning, expeditious weaning

 Limit airway and/or plateau pressures.

 Limit excessive diuresis; limit excessive use of PEEP

 Continuous monitoring of level of paralysis with train of four stimulation.

 Titrate sedation according to sedation assessment scale.

 Careful attention to appropriate central line placement technique.

 Most abnormalities of pulmonary function that occur within the first two weeks of extubation significantly improve over the next six months. The degree of impairment and the level of improvement over time in forced vital capacity correlate with the severity of lung injury.

Pulmonary embolism (PE)

It is a relatively rare but potentially fatal complication that accounts for 1–4% of all deaths after cardiac surgery. When sudden unexplained circulatory collapse occurs, pulmonary embolism should always be considered.

Risk factors for pulmonary complications

After cardiac surgery with cardiopulmonary bypass, pulmonary complications are common complications. Postoperative pulmonary complications occur early as arterial hypoxemia, later as pneumonia, and rarely as acute lung injury as well. Post-operative pulmonary complication incidence ranged from 3-16% after grafting of the coronary artery and from 5-7%.

An important risk factor for postoperative pulmonary complications was preoperative congestive heart failure. The atrial hypertension and pulmonary interstitial edema were often left in patients with congestive heart defect preoperative, causing a pulmonary ventilation / blood flow ratio change and thus postoperative hypoxemia and prolonged ventilation support. The lymph was back on preoperative congestive heart failure, and pulmonary alveolar edema occurred, which could in turn have changed pulmonary conformity and further worsened respiratory disorder. Thus, preoperative congestive heart failure patients were prone to complications of the pulmonary complications. A proper pre-operative control of congestive heart failure could therefore help reduce the incidence of postoperative pulmonary complications in patients undergoing scheduled heart surgery with CPB. In patients, low preoperative PaO2 often suggested poor cardiopulmonary function or severe chronic pulmonary obstructive disease. Following cardiac surgery with CPB, further reduction in cardiopulmonary function was expected in patients with low preoperative PaO2 who were therefore more prone to low cardiac output and required longer ventilation support and were therefore more prone to postoperative complications of the pulmonary system. Therefore, proper periopulmonary dysfunction management may help improve cardiopulmonary function and shorten postoperative ventilation support, and then reduce the incidence of postoperative pulmonary complications.

Also a major risk factor for postoperative pulmonary complications was prolonged cardiopulmonary bypass. CPB is associated with a systemic inflammatory response, the production of oxygen-generated free radicals, the activation of polymorphonuclear neutrophils, and the cascade of supplements and the release of constrictive vessel factors. All of these affect important organs, such as the heart, lung, brain, and kidney, negatively. It was expected that prolonged cardiopulmonary bypass would negatively affect cardiopulmonary and renal functions, thus requiring longer ventilation support and increasing postoperative pulmonary complications. Moreover, prolonged cardiopulmonary bypass associated with complex disease, complicated surgery and imperfect myocardial protection may cause postoperative pulmonary complications. Therefore, further refinement of surgical techniques and decreased cardiopulmonary bypass duration can contribute to reducing post-operative pulmonary complications.

Older age was one of the major risk factors contributing to complications of the postoperative pulmonary. Patients over 65 years of age undergoing cardio-operative surgery with CPB have often experienced multiple concurrent cardiopulmonary reserve diseases. After cardiac intervention, they were further reduced in cardiopulmonary performance and more inclined to low heart output postoperatively and needed a longer ventilation support, and were then more prone to pulmonary complications after surgery.

The incidence of phrenic nervous injury following cardiac surgery varied according to the diligence sought. Finite studies have shown that this complication is linked to cold-induced injury in myocardial protection and possibly mechanical injury during mammalian inner arteries harvest. Right, though rarely life threatening, phrenic nerve injury was more likely to cause diaphragm paralysis, atelectasis, serious pulmonary dysfunction requiring prolonged mechanical ventilation or re-intubation, and related morbidity, and even mortality. Correct phrenic nerve injury was an independent risk factor for respiratory complications after surgery. Bilateral phrenic nerve injury, although rare, can lead to pulmonary post-operative complications.

MANAGEMENT

Pneumonia, aspiration pneumonitis, respiratory failure, reintubation within 48 hours, weaning failure, pleural effusion, atelectasis, bronchospasm, and pneumothorax are among the different conditions that include postoperative pulmonary complications. The incidence rates of post-operative pulmonary complications vary from 2% to 40%, depending on context. These events increase mortality, length of stay post-operative, ICU admissions, hospital readmissions, and expenses. Postoperative pulmonary complications -associated mortality varies, but in some contexts it can reach as high as 48%. In patients with postoperative pulmonary complications, ICU admission levels are between 9.5% and 91% higher. Strategies to reduce the impact of modified risk factors include alcohol and self-restraint from smoking before surgery, shorter surgery duration, physiotherapy and techniques of encouragement spirometry; however, they are currently being supported with little scientific evidence [2].

The semirecumbent position (30–45°elevation of the bed head) protects against pulmonary aspiration and reduces bacterial contamination of the airway. It can also reduce VAP incidence. This simple intervention's success depends on compliance with ICU staff. In addition, biochemical and bacteriological markers show that, despite head-lifting, orogastric contamination of aviation continues, with VAP still being present at significant rates despite broad semi-recumbent positions.

Some studies show potential benefits from both lateral and prone positions and rotational therapy. However, each of these positions presents major challenges over the post-operative period and none have shown superiority over the semi-level position. Reduce the incidence of VAP, ICU LOS and, if possible, mortality by minimizing continuous intravenous sedation in patients with mechanical ventilation and removal of the endotracheal tube. Minimizing sedation can be achieved by a daily breech of the infusion in patients receiving traditional agents as midazolam, propofol, or morphine while ensuring that the patient is awake, comfortable, and able to follow instructions. It is possible to achieve earlier removal of the endotracheal tube by incorporating daily spontaneous breathing tests until the patient is able to breathe for 2 hours without ventilation support.

Early use of NIV reverses atelectasis-induced post-operative hypoxemia, limits the need for tracheal reintubation, and may decrease PP rates compared to oxygen alone administration. A variety of interfaces can achieve NIV, including a mouthpiece, nasal, face, or helmet mask. Despite its shown advantages, NIV in operating patients is much less common than in medical patients, largely because of its concerns about their safety following abdominal surgery and the administration of sedative drugs. However, recent reports show that after careful scrutiny for possible contraindications the proper use of experienced providers makes non-invasive ventilation safe and effective. Finally, to minimize the transport of intubated patients, any interference with ICU treatment during maneuvers which could compromise the correct screening of an endotracheal tube cuff is avoided. Preventing unnecessary trips outside the ICU is cost efficient, limits interference with scheduled care and can reduce VAP incidence.

In the operating room, measures to prevent VAP should be initiated and continued at the ICU. These include general infection control measures like fastidious hand washing, adequate antibiotic use, and proper oral hygiene and airway management. The routine after surgery to manage oropharyngeal secretions include patient mobilization, humidification of the airway, sucking through the tube, intermittent stimulation of the cough and external application of manual ribcage compression to enhance the elimination of secretions. The preventive measures included hand care, glove and cloth usage, lifting backrest, maintaining tracheal manguet pressure, the use of orogastric tubes, preventing gastric over distance, good oral hygiene, and removing non-essential tracheal suction. VAP rates decreased by 43%. Despite the high compliance with preventive measures, the rates were still considerable, which suggests that the complete elimination of VAPs from ICU could be a very difficult goal.

In addition to intraoperative protective ventilation strategies and appropriate management of neuromuscular blocking drugs, preventive measures include co-morbidity optimization, smoking

cessation, and anaemia correction. Low tidal volumes must be calculated on the basis of an ideal body weight for the patient, and Protective ventilation.

Protective ventilation

Until the patient was extubated or died, protective or conventional mechanical ventilation was rigorously maintained. Each patient was connected to a closed system for aspiring tracheal secretions; during aspiration, the patient remained connected to the ventilator, minimizing temporary airway pressure drops. The target partial pressure of arterial oxygen in both groups was 80 mm Hg, and the level of PEEP was never set below 5 cm of water, even during the ventilator weaning. In the two groups, the weaning procedure was the same: a gradual decrease in pressure support level. Patients were ventilated exclusively by endotracheal tube.

 Breathing mechanics maneuver that records a quasi-static pressure / volume curve.

 Easy to evaluate recruitability of ARDS patients.

 Simple and safe way to perform lung recruitment maneuvers.

 Can be combined with the measurement of esophageal pressure.

All patients were subjected to the following before cardiac surgery:

(2) Radiography of the chest and EGG.

(3) Complete blood picture and serum potassium and sodium. (4) Blood urea and serum creatinine.

(5) Blood sugar fasting.

(6) Serum bilirubin, albumin, SGOT and SGPT. (7) Time, concentration, and INR of the prothrombin.

All patients were followed up for the following after cardiac surgery:

(2) Time for coronary bypass. (3) Cross clamp time.

(4) Ten days follow up in the hospital and 1 month after discharge. (5) Intraoperative complications and blood transfusion.

(6) Complications after surgery

(7) Time of post-operative complications.

(8) Post-operative ECG, chest X-ray, complete blood picture, blood urea, serum creatinine, serum potassium and sodium. Prothrombin time, concentration and INR.

(9) Amount of post-operative blood transfusion. (10) Analysis of blood gas.

(11) Management of complications and outcome patients.

(12) Trans-tracheal aspiration, gram stain and culture cases of pulmonary infection.

Criteria for diagnosis of post-operative pneumonia:

(2) New chest radiographic shadow.

(3) New onset radiographic shadowing, progressive inflation, consolidation, cavitations or effusion. (4) Organism isolated from sputum obtained by trans-tracheal aspiration.

Criteria for diagnosis of acute respiratory distress syndrome:

(3) Reduced total lung compliance less than 50 ml/cm H2O.

(4) No evidence of heart failure by clinical examination and echocardiography [9].

Hypoxemia

Measured by arterial blood gases. Hypoxemia is defined as an arterial blood gas value PaO2 of less than 60mmHg, represents low blood oxygen level and low hemoglobin saturation. Acute hypoxemia may cause dyspnea, restlessness, and anxiety. Signs include confusion or alteration of consciousness, cyanosis, tachypnea, tachycardia, and diaphoresis. Cardiac arrhythmia and coma can result. Inspiratory opening of closed airways causes crackles, detected during chest auscultation; the crackles are typically diffuse but sometimes worse at the lung bases, partic ularly in the left lower lobe. Jugular venous distention occurs with high levels of positive end-expiratory pressure (PEEP) or right ventricular failure.

Mechanical ventilation if saturation is < 90% on high-flow oxygen underlying conditions must be addressed as discussed elsewhere on the site. AHRF is initially treated with high flows of 70 to 100% oxygen by a nonrebreather face mask. If oxygen saturation > 90% is not obtained, mechanical ventilation probably should be instituted. Specific management varies by condition. In up to 30% of ARDS patients, severe hypoxemia is associated with higher mortality and longer mechanical ventilation duration.

Causes of hypoxemia,

 Inadequate O2 delivery

 Patient: acute lung pathology (atelectasis, collapse, pneumothorax, haemothorax,)

 Endotracheal tube malposition or not patent

 Measurement problem

 Inadequate cardiac output

Management of hypoxemia:

Patient with ARDS are severely hypoxemic. Option available for improving arterial oxygen saturation (spo2) includes:

 Use of high fractions of inspired oxygen(Fio2)

 Exclude equipment failure and malposition of tube

 Drain pneumothorax or pleural fluid

 Improve oxygen delivery

 Optimise cardiac output

 Manipulate mechanical ventilator support.

 Bronchodilators

 Lung protective ventilation

 Consider antibiotics if indicated

These options are most frequently applied in combination.

PaO2/FIO2

The PaCO2 is the respiratory component of the arterial blood gas. The normal value is 35-45 millimeters of mercury (mmHg). An increase in PaCO2 indicates decreased ventilation of the alveoli. A decrease in PaCO2 indicates hyperventilation Gas exchange is commonly used to define respiratory failure and the degree of lung dysfunction / injury in the absence of a direct, reliable marker for lung injury [34]. The PaO2/FIO2 ratio is the most commonly reported index of gas exchange impairment for hypoxic respiratory failure in general and ARDS in particular.

ABG’s

 Metabolic alkalosis- PH is >7.45 and HCO3 >26mEq/L

 Metabolic acidosis- PH is <7.35 AND HCO3 <26mEq/l

 Respiratory alkalosis- PH is >75 and CO2<35

 Respiratory acidosis- PH is <7.35 and CO2>45

 A decreased pH (less than 7.35) always indicates acidosis.

 An increased pH (greater than 7.45) always indicates alkalosis.

Mechanical Ventilation

Mechanical ventilation is indicated when the patient's spontaneous breathing is inadequate to maintain life. It is also indicated as prophylaxis for imminent collapse of other physiologic functions, or ineffective gas exchange in the lungs [34,33]. Because mechanical ventilation serves only to

provide assistance for breathing and does not cure a disease, the patient's underlying condition should be identified and treated in order to resolve over time.

Indications for Mechanical Ventilation Respiratory Abnormalities

There are clinical assessments, loss of ventilatory reserve, and refractory hypoxemia that may suggest mechanical ventilation. Clinical Assessment: Apnea, stridor, severely depressed mental status, flail chest, inability to clear respiratory secretions, trauma to mandible, larynx, or trachea [34]. Loss of Ventilatory Reserve: Respiratory rate >35 breaths/min, tidal volume 10 mmHg. Refractory Hypoxemia: Alveolar-arterial gradient >450, PaO2/PAO2 <55mmHg.

Nursing Care Considerations for the Intubated Patient

• Assess ventilator settings, alarms, and patient’s ability to synchronize breathing with the ventilator. • Gloves and hand washing should be used for every contact with the ventilator.

• Monitor patient for increased heart rate, mental status change, respiratory rate, diaphoresis, or other signs and symptoms of increased work of breathing.

• Use a dry erase board, pen and paper, or open letter board for communication if appropriate. • Patient should be kept nil by mouth (NPO) while intubated. This includes ice chips.

• Suction according to patient need.

• Continuous monitoring of EKG and oxygen saturation.

• Maintain equipment at the patient’s bedside: complete suction setup, 10 mL syringe for cuff inflation/deflation, Bag-Mask-Ventilation (BMV) System, tracheostomy tube of same size as indicated and one size smaller (for tracheostomy patients), and oral care.

• For tracheostomy patients, the nurse will provide care to clean the tracheostomy tube and stoma site; change the securing device, and remove the inner cannula and clean if appropriate as per nursing standard of care.

• All mechanically ventilated patients receiving sedation will be assessed for appropriateness of sedation wake up and readiness to wean.

• Maintain standard precautions and utilize appropriate PPE. Wear face shields for any procedure which may cause the release of fluids (suctioning, tracheostomy care, etc.).

• General observations at the bedside every hour to assure proper ventilation and oxygenation per nursing standard of care.

• Monitor lung sounds, ETT placement, and cuff leaks regularly.

• Assess ventilator settings, alarms, and patient’s ability to synchronize breathing with the ventilator.

PEEP

PEEP is an essential mechanical ventilation component for ARDS patients as it was found early that PEEP greatly improves oxygenation in ARDS patients. High levels of PEEP can open collapsed alveoli and lower intrapulmonary shunting [34]. Additionally, by decreasing alveolar overdistance, ventilation-induced alveolar injury is reduced, because more open alveoli share the volume of each subsequent tidal breath. On the other hand, high PEEP levels during the respiratory cycle can decrease repetitive alveolar opening and closing, thereby promoting lung injury.

Recruitment maneuvers

A recruitment maneuver is a transient increase in trans-pulmonary pressure to reopen collapsed alveoli. The recruitment techniques described include continuous high-pressure inflation and increased PEEP, while reducing the tidal volume, but it is unclear whether there is superior maneuver to others [33]. Several studies have shown improved gas exchange with recruitment maneuvers, but no RCT has shown benefits on ARDS mortality and hypotension and decreased saturation occurs in 12% and 8% of patients during or after such maneuvers respectively. Although routine recruitment maneuvers are not recommended in ARDS, based on currently available data, these maneuvers in patients with life-threatening refractory hypoxia may dramatically improve their oxygenation and should be seen as rescue therapy.

Physiotherapy

Patients undergoing heart surgery in many countries are offered physical therapy. Limited data are published concerning physical therapy and exercises for patients after cardiovascular operations in Europe.

The patients usually were treated for 1 to 6 sessions a day by the physical therapist during the first post-operative days. The normal postoperative physical therapy treatments were breathing, coughing, vibration of the thorn wall and mobilization. According to 91% of physical therapists, coughing support was provided for patients. The most common technique was manual cough support by the physical therapist. In total, 93% of physiotherapists instructed the patients to conduct regular

post-operative breathing exercises. The two most commonly used techniques were deep breathing exercises and incentive spirometry [11]. Post-operatively, recommendations were made on the continuation of breathing exercises during three days to eight months.

As a preventive measure for lung protection, preoperative prophylactic physiotherapy with inspiratory or expiratory muscle training can be used. Postoperative physiotherapy is used prophylactically in patients undergoing heart surgery. During this period, various techniques can be used to improve air-perfusion inequalities, increase pulmonary compliance and help to reinflate the collapsed alveoli. These techniques include deep respiratory exercises, slow maximum inspiration with an inspiring hold, intermittent deep respiratory exercises with and without an incentive spirometer, and deep respiratory exercises with expiratory resistance.

During the hospital stay, pre-and postoperative physical therapy treatment is often prescribed to patients with cardiac surgery to prevent or decrease postoperative complications. The treatment for physical therapy consists of early mobilization, range of exercises in motion, and exercises in breathing. There is agreement on the value of early mobilization, but there is limited scientific evidence on how to mobilize and exercise the surgical patient during the first days after surgery. After cardiac surgery, various respiratory techniques are recommended with or without mechanical equipment, but controversies arise concerning the most effective respiratory techniques.

The physiotherapist usually gave patients one to 6 treatment sessions a day during the first five days after surgery. Almost all physical therapists regularly recommended breathing and coughing exercises after surgery. The two most common techniques are deep breathing and incentive spirometry.[10] Sternal care has been taken regularly, but it is advised that patients should avoid weight bearing as long as after the operation.

Coronary artery disease (CAD) is one of the leading causes of death in developed countries, where obesity and lack of physical activity are key factors in its increasing impact. The advantages of CABG operation with regard to survival and improved ventricular function are well known, but there is a risk for post-operative pulmonary complications (PPCs) such as pneumonia, atelectasis, breathing failures, Pneumothorax or bronchospasm, as is the case with many other cardiac intervention. [18]. While overall mortality from these complications have fallen in recent years, these continue to have a strong connection with patient morbidity, resulting in longer hospitalization times that have consequences for patients, families and increased healthcare expenditures. Besides the physical impact, literature shows the presence as anxiety of psycho-emotional results. Physiotherapy is a treatment option both in pre-operative and postoperative treatment, and many hospitals have

physiotherapists specialized in helping these patients through practice, education, and support physically and emotionally. However, not all patients are treated with or are not prescribed for physical treatment in the preoperative stage.

In high-risk patients, prophylactic maneuvers should be encouraged to reduce the incidence and magnitude of postoperative atelectasis. These techniques include deep respiration, coughing and spirometric incentives. Prophylactic measures should be taught and instituted before surgery for the maximum benefit and used regularly after surgery, on an hourly basis. After surgery, early patient ambulation is as effective as physical therapy. Postoperative atelectasis is treated with sufficient oxygenation and lung segment re-expansion. Additional oxygen should be treated to achieve a saturation of arterial oxygen exceeding 90%.

Atelectasis treatment depends on the etiology underlying it. To treat acute atelectasis, including postoperative lung collapse, the underlying cause must be removed.

Prevention is the best approach for post-operative atelectasis. Post anesthesia-related anesthetic agents should be avoided. Sparingly, narcotics should be used because they depress the reflex of cough. It is important to ambulate early and use incentive spirometry. Encourage cough and deep breathing for the patient. Nebulized bronchodilators and moisture can help to liquefy secretions and facilitate their removal. In the case of lobar atelectasis, vigorous therapy of the chest often helps to re-expand the lung that has collapsed. Flexible fiberoptic bronchoscopy could be performed if these efforts are not successful within 24 hours. Further atelectasis is prevented [1] by placing the patient in a position to promote increased drainage of the affected area, [2] by vigorous chest therapy, and [3] by encouraging the patient to cough and to breathe deeply.

Prone position

In patients with acute lung injury (ALI)/acute respiratory distress syndrome (ARDS), prone positioning has been used for many years.It Improve oxygenation in patients requiring mechanical ventilation support for acute respiratory distress syndrome (ARDS) management. Randomized, controlled studies have confirmed that oxygenation is significantly better when patients are in the prone position than when they are in the supine position. In patients with an arterial oxygen tension (PaO2)/inspiratory oxygen f

raction (FIO2) ratio <100 mmHg, meta-analysis suggested better survival. Prone positioning improves lung compliance and ventilation-perfusion matching by reducing the posterior atelectasis lung. This is because the heart and anterior lung field are placed down, instead of acting with gravity

to compress the large posterior lungs. Therefore more of the lung parenchyma is ventilated, and at a fixed tidal volume the lung will suffer less barotrauma.

Placing a patient in the prone position requires significant effort and has serious risks, close attention to lines, drains, and airway is critical, as is obsessive attention to pressure point padding and prevention of ulcer [30]. Prone position ventilation is a safe strategy and reduces mortality in patients with severely impaired oxygenation. It should be started early, for prolonged periods, and should be associated to a protective ventilation strategy.

The prone position offers clinical advantages such as improved oxygenation by optimizing lung recruitment and ventilation-perfusion ratio, and is also likely to prevent and reduce ventilator-associated lung injury by homogenizing stress and stress on the lung parenchyma, resulting in a reduction in mortality risk. Based on the results obtained, the prone position can be recommended in patients with severe hypoxemia (PaO2/FiO2<100), associated with low tidal volume (< 8ml / kg ideal weight), over a period of more than 16h a day, and beginning early during disease (< 48h) [30,31]. These would therefore be the indications and associated strategies to be included in the protocols for pronation. Pronation does not require special equipment, but should be performed by trained personnel and take the necessary safety measures to avoid complications associated with it. The fact that prone positioning improves mortality in patients with severe ARDS is now supported by a large body of evidence. Pronounced positioning should therefore be used as first-line therapy.

ORGANISATION AND METHODOLOGY OF RESEARCH

The literature search was performed in the databases Pubmed, Science Direct, PLOS Google Scholar. Reviewed more than 40 literature reviews, published between 2009-2019. The analysis of the case report and the PICO questionnaire method is thoroughly performed in the literature review.

CASE STUDY

A 77-year-old man (Mr. JS) with triple coronary artery disease has undergone on-pump coronary artery bypass surgery (CABG). The standard general endotracheal anaesthesia was performed. Postoperative management - standardized and adopted by that clinic. Mechanical ventilation (MV) on SIMV mode (synchronized intermittent-mandatory ventilation) was applied. The patient was hemodynamically stable, with minimal bleeding and adequate diuresis.

Chest X-ray showed possible atelectasis on the left, that treatment used applied Continuous Positive Airway Pressure mode (CPAP). Observing good vital parameters, four hours after arrival at ICU decision to extubate this patient was made. Patient’s oxygen therapy over high flow nasal cannulae (NC) was continuing, with FIO2 of 0.4. On six hours after surgery follow-up, the patient developed increasing oxygen, requirements revealed hypoxemic respiratory failure. Diagnostic Findings - arterial blood gas (ABG) results: pH 7.35, PaO2 59 mm Hg, PaCO2 37 mm Hg, bicarbonate 16mEq/L, Sat O2 89%, while FIO2 of 0.6 through an NC. Initially, he is receiving 65-70% O2 through an aerosol facemask (FM), than his oxygen saturations improved to the mid-90% range on an, in the past two hours, the nurse has had to increase the FIO2 to 0.7 and his Sat O2 is still in the lower 90% range. The patient’s repeated chest x-ray has shown visible reflex atelectasis slight increase on the left and pulmonary edema. An echocardiogram revealed normal left ventricular function. His blood pressure (BP) with a tendency to decrease 100/60 mm Hg and his heart rate (HR) 120 bts/min., some signs of tissue hypoxia developing. Respiratory failure in progresses, tachypnea, tachycardia, auxiliary muscles are involved in breathing. Therefore, the nurse drew an ABG which shows pH 7.30, PO2 51, pCO2 22, HCO3- 22, Sat O2 89% on an FIO2 of 0.8 through an FM. The patient require nasotracheal suctioning, nebulized bronchodilators and chest physiotherapy to helps re-expand the collapsed lung segments.

Negative dynamics evolved: acute lung insufficiency (ALI) progressed dynamics, sharp oxygen therapy was used, which later shifted to CPAP mode delivered via a facemask, but two hours later there is no improvement and the patient was re-intubated. MV started on the Drager Infinity C500 ventilator with SIMV mode, FIO2 of 0,8, rate 12 bpm and positive end expiratory pressure (PEEP) 5-10 cm H2O, applied reqruitment maneuvers. The patient was sedated with propofol to improve tolerance of MV and decrease oxygen consumption. Applied conservative fluid management strategy to minimize positive fluid balance. Repeated chest x-ray, fiberoptic bronchoscopy (FBS) has been done - bronchi are free, secretion is low.

On the next postoperative day ALI with prolonged MV requirement was observed. PaO2/FiO2 ratio significantly decreased and was128 mmHg (partial pressure of arterial oxygen / fraction of inspired oxygen ratio) with a FiO2 0.7 and PEEP 5 cm H2O. Was applied open lung ventilation (OLV) strategy that combines low tidal volume ventilation (LTVV) with a recruitment maneuver.

The patient was hemodynamically stable, however BP 90/60 mmHg. Chest x-ray shows new scattered interstitial infiltrates compatible with an ARDS pattern as interpreted by the radiologist.

On the third postoperative day oxygen demand increased, Sat O2 reached 90%, PEEP increased to 10-12 mm H2O, developed refractory hypoxemia, PaO2/FiO2 ratio further decreased - 67 mmHg. The patient's condition is evaluated as acute respiratory distress syndrome (ARDS) with persistent hypoxia request for high FiO2 and his was transferred on the Drager Evita 4ed ventilator with airway pressure release ventilation (APRV) mode.

On postoperative day fifth enlarged inflamatory inndex was observed. Chest X-ray showed left basal consolidation and infiltration. It was developed a nosocomial infection - pneumonia, which was established causative agent: Klebsiella pneumonia was grown from sputum. Antibiotic therapy was applied with broad-spectrum intravenous antibiotics. During this period the patient was on continued supportive care, including intelligent use of sedatives and neuromuscular blockade, hemodynamic management, nutritional support, control of blood glucose levels, expeditious evaluation and treatment of nosocomial pneumonia, and prophylaxis against deep venous thrombosis (DVT) and gastrointestinal (GI) bleeding.

In order to improve the evacuation from the airways, suctioning and FBS were performed. For the same purpose, the patient was prone positioned twice per day. He responded well to prone positioning (PP) with the PaO2 increasing to 100.

The patient’s condition remained critical for 15 days in ICU due to ARDS and pneumonia with the need of prolonged MV. The patient’s condition improved gradually. On postoperative day 16 his condition stabilized, returned to ventilation on the Drager Infinity C500 ventilator with SIMV, FIO2 of 0,7, rate Spontaneous breathing was adequate and on the day 20 he has been able to be separated from the ventilator 12 bpm and PEEP 5-10 cm H2O. By 16 days post-admission, he was able to tolerate CPAP. After extubation, oxygenation using mask with a reservoir was continued, intermittently applying CPAP mode. Afterwards – nasal canullae (NC).

In post-extubation period the patient was weak and hypoactive, needed medical staff help but he was consiscious, his vital functions were adequate.

In summary, the patient required ventilatory support for 20 days. Length of stay in ICU was 32 days, length of hospital stay – 40 days.

DISSCUSSION

Cardiac surgery, especially when performed using CPB, results in major disturbances in body homeostasis, including major changes in the structure and function of the respiratory system. Weissman et al [9]. Atelectasis forms immediately upon the induction of general anesthesia, positive pressure ventilation alerts. The postoperative period offers further challenges, including pain and mechanical ventilation. Given that many patients undergoing cardiac surgery have underlying lung disease or a history of smoking, it is remarkable that more patients do not suffer major pulmonary complications during and after cardiac surgery. Advances in anesthetic, surgical, and critical care have, reduced the physiologic insults of surgery and streamlined care in the immediate postoperative period (e.g., early extubation). Moreover, the development of minimally invasive surgery and nonbypass techniques are further evidence of the attempts at reducing the homeostatic disruptions of cardiac surgery. Naveed et al [4] Most common postoperative pulmonary complication was atelectasis, respiratory failure, pneumonia and acute respiratory distress syndrome. The main risk factor of

Postoperative pulmonary complications were advance age ≥ 60 years, prolonged CPB time (CPB time > 120 minutes), pre-op pulmonary hypertension and intraoperative phrenic nerve injury are independent risk factors of postoperative pulmonary complications after surgery. J. Verhij a et al [10], After cardiovascular surgery, mild pulmonary oedema is generally normal, even without high filling pressures, and is for the most part attributable to a low COP, independent of expanded penetrability in around one-half of patients. It might prolong mechanical ventilation. Be that as it may, pneumonic radiographic and ventilatory anomalies may result, at any rate to some extent, from atelectasis instead of increased oedema.

The course of events from pulmonary dysfunction associated with surgery to discharge from the hospital in cardiac patients is largely unexplored. Wynne R, Botti M et al [14]. In the absence of evidence-based practice guidelines for the care of cardiac surgical patients with postoperative pulmonary dysfunction, an understanding of the pathophysiological basis of the development of postoperative pulmonary complications is fundamental to enable clinicians to assess the value of current management interventions. Previous research on postoperative pulmonary dysfunction in adults undergoing cardiac surgery is reviewed, with an emphasis on the pathogenesis of this problem, implications for clinical nursing practice, and possibilities for future research. Christopher Noel et al [12], The most frequent pulmonary consequence of cardiac surgery is atelectasis, seen on postoperative chest radiographs in approximately 50% to 90% of patients. The course of events from

pulmonary dysfunction associated with surgery to discharge from the hospital in cardiac patients is largely unexplored. In the absence of evidence-based practice guidelines for the care of cardiac surgical patients with postoperative pulmonary dysfunction, an understanding of the pathophysiological basis of the development of postoperative pulmonary complications is fundamental to enable clinicians to assess the value of current management interventions. Previous research on postoperative pulmonary dysfunction in adults undergoing cardiac surgery is reviewed, with an emphasis on the pathogenesis of this problem, implications for clinical nursing practice, and possibilities for future research.

The rate of Postoperative pulmonary difficulties after cardiovascular medical procedure was high, Main result was the advancement of atleast one of the accompanying: respiratory disappointment, respiratory contamination, bronchospasm and atelectasis, Significant autonomous hazard factors for PPC were: age >80 years, weight >30 BMI, preoperative SpO2< 96% [27]. Pneumonic inconveniences are basic after coronary artery bypass grafting. Distinguishing those people with expanded risk of pulmonary complications takes into consideration fitting preoperative mediation. The most usually observed aspiratory confusions incorporate pleural emission, hemothorax, atelectasis, aspiratory edema, diaphragmatic dysfunction and pneumonia.

Pulmonary complications following cardiac surgery with cardiopulmonary bypass are common complications Qiang Ji et al, [15]. Postoperative pulmonary complications manifest early as arterial hypoxemia, during the later course as pneumonia, and in rare cases also as acute lung injury. The incidence of postoperative pulmonary complications ranged from 3-16 percent following coronary artery bypass grafting and 5-7 percent following cardiac valvular surgery. In this study, 143 adult patients suffered from postoperative pulmonary complications, accounting for 6.96% of the total population. Postoperative pulmonary complications (PPC) occur frequently in cardiac surgery Johannes F.H. Ubben et al [16]. The incidences vary from 10% to 25%, 1–3 and at least 2% to 5% of all patients undergoing cardiac surgery are at risk to develop a severe postoperative lung dysfunction, such as an acute respiratory distress syndrome. Postoperative pulmonary complications lead to pro- longed hospital stays and increased costs. Data from autopsy reports suggest that 5% to 8% of cardiac surgery-associated mortality could be related to respiratory complications. Prolonged postoperative ventilation is associated with an increased risk for PPC and should be avoided if possible. A fast- track anesthetic regimen with the use of shorter acting drugs may help in reducing ventilator times Pulmonary dysfunction is a significant cause of morbidity following cardiac surgery Frank E Silvestry et al, [10]. Common types of pulmonary dysfunction include pleural effusion, pneumonia, atelectasis, decreased thoracic compliance, difficulty weaning from mechanical ventilation,